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exercise physiology Flashcards

1
Q

what are the types of exercise?

A

dynamic

static

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2
Q

define dynamic exercise. give examples

A

rhythmical movement of joints and contraction and relaxation of muscles. Swimming, running & cycling.

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3
Q

define static exercise. give examples

A

maintained contraction for a length of time. Weight-lifting

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4
Q

what ATP supply is the immediate energy system? what is its function?

A 
fastest supply of ATP - creatine phosphate (phosphocreatine)
function - rapid mobilisation of high energy phosphates. uses no O2
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5
Q

what ATP supply does anaerobic glycolysis provide? what is its function?

A

can supply ATP when requirements are high

less efficient at making ATP. uses no O2.

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6
Q

what ATP supply does oxidative metabolism provide? what is its function?

A
  • sustained supply of ATP

- function; uses O2

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7
Q

what are the 3 sources of metabolism that support skeletal muscle function?

A
  1. Immediate
  2. Non-oxidative
  3. Oxidative (aerobic)
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8
Q

where are high concentrations of creatine phosphate found?

A

in the muscles

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9
Q

what is the function of creatine phosphate?

A

• Provides a store of high potential phosphate to maintain contraction

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10
Q

what is phosphocreatine broken down to and what catalyses this reaction?

A

• Phosphocreatine  creatine produces ATP

o Catalysed by creatine kinase

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11
Q

how is ATP generated in anaerobic glycolysis?

A

ATP generated from glucose via the glycolytic pathway – less efficient at making ATP

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12
Q

what causes muscles to fatigue?

A
  • Excess pyruvate  lactate
  • Lactic acid build-up
  • Drop in pH – muscle begins to fatigue
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13
Q

where is energy derived from in sustainable exercise?

A

aerobic metabolism

need O2

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14
Q

what is VO2?

A

the rate of O2 uptake by skeletal muscle (amount of O2 consumed)

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15
Q

what equation can determine VO2?

A

VO2 can be determined by the Fick equation

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16
Q

what is Fick’s equation? define each term

A

VO2 = Q x (CaO2 – CvO2)

Q – cardiac output of the heart (blood flow to muscle)
CaO2 – arterial oxygen content
CvO2 – venous oxygen content
(CaO2 – CvO2) is also known as the arteriovenous oxygen difference

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17
Q

what is the VO2 in a 70kg person?

A

250ml/min

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18
Q

how much O2 is consumed/min/kg body mass?

A

3.6ml/min/kg of body mass

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19
Q

what is VO2 max?

A

– highest peak O2 uptake obtained during dynamic exercise using large muscle groups during a few mins performed under normal conditions at sea level

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20
Q

when is VO2 reached?

A

when O2 consumption remains at a steady state even in an increase in workload

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21
Q

what does VO2 show?

A

Reflects aerobic physical fitness of the individual – important determinant of endurance capacity during prolonged, sub-maximal exercise

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22
Q

what is the anaerobic threshold?

A

point where lactate begins to accumulate in the bloodstream

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23
Q

how does lactic acid reduce exercise endurance?

A

Lactic acid produced faster than it can be metabolised  metabolic acidosis  exercise endurance = reduced

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24
Q

would elite athletes have a high or low anaerobic threshold?

A

high

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25
what are the 2 major consequences of increased exercise?
* Rise in cardiac output – through increases in SV and HR | * Redistribution of larger proportion of cardiac output to the active muscles
26
how is HR kept low?
action of the parasympathetic nervous system (vagus nerve)
27
how are HR and SV increased at the start of exercise?
* As exercise begins, there’s reduced activity of the parasympathetic nerves and increased activity of sympathetic nerves * Increased HR and mobilisation of blood from great veins (vasoconstriction) * Increased venous return  Increased EDV (increased preload)  increased SV * Sympathetic activity has a positive inotropic response to the heart
28
define hypertrophy
increase in cardiac myocyte size to increase muscle mass
29
how can hypertrophy of the heart muscle occur?
physiologically | pathologically
30
how can physiological hypertrophy occur?
pregnancy or exercise
31
how are the left ventricles affected for; - endurance athletes - strength athletes - combination athletes?
 Endurance athlete – thickening of LV walls  LV dilation  Strength athlete  mild LV dilation  Combination athlete  gross thickening of LV walls  LV dilation
32
how can heart muscle hypertrophy occur pathologically?
 Hypertension – thickening of LV walls  no dilation in early stages of disease  Dilated cardiomyopathy, heart failure  thinning of LV walls  significant LV dilation  Hypertrophic cardiomyopathy  gross thickening of LV walls  no dilation/decrease in LV chamber size
33
what physiological remodelling occurs in an athlete's heart? is it reversible?
o Increased muscle mass o Normal cardiac function o Reversible
34
what physiological remodelling occurs in a failing heart? is it reversible?
o Increased muscle mass o Reduced cardiac function o Irreversible o Cell death and fibrosis
35
how does volume-induced cardiac hypertrophy occur?
increases resting EDV and SV
36
how does the HR of athletes compare to untrained individuals?
athletes have bradycardia
37
at rest, what % of resting CO is distributed to the muscles?
20-25%
38
during maximal exercise, how much of the increased CO goes to the muscle?
80-90%
39
what mechanisms control redistribution of blood flow?
systemic regulation | local control
40
how does systemic regulation control distribution of blood flow?
* Start of exercise – increase in sympathetic outflow to the heart and systemic resistance vessels * Adrenergic receptors play an important role directing blood flow from non-essential organs to skeletal muscle
41
what do alpha adrenoreceptors do?
constrict vessels in the gut - cause vasoconstriction of veins
42
what do beta-1 adrenoreceptors in the heart do?
increase rate and force of myocardial contraction
43
what do beta-2 adrenoreceptors do?
relax smooth muscle and increase ventilation + oxygen uptake and cause vasodilation of blood vessels, esp those supplying skeletal muscle
44
where do local regulatory factors that control blood flow come from?
blood vessels themselves | surrounding tissue
45
what local regulatory factors come from the blood vessels?
endothelial factors and myogenic mechanisms e.g. NO relaxes smooth muscle and causes dilation of blood vessels
46
what local regulatory factors come from the surrounding tissue?
tissue factors. E.g. adenosine and inorganic phosphates, carbon dioxide, hydrogen ions (H+) and potassium ions (K+) released from contracting muscles
47
how does increasing vasodilator metabolites increase muscle blood flow?
decreases TPR which increases skeletal and cardiac muscle blood flow
48
how do you calculate MAP?
MAP = (CO x TPR) + CVP
49
why does MABP rise only slightly in exercise?
decrease in TPR is counteracted by increases in CO
50
how does systolic pressure change in exercise and why?
increases bc of increase in ventricular contraction force
51
how does diastolic pressure change in dynamic exercise?
stable/decreass slightly
52
how is the body's increased need for O2 met?
met through increased pulmonary minute ventilation and oxygen extraction in tissues
53
what is the pulmonary ventilation at rest?
8L/min
54
what is the pulmonary ventilation during heavy exercise?
100L or more
55
what causes the increase in minute ventilation in exercise?
increase in resp rate | increase in tidal volume
56
how is O2 taken up into the lungs?
pulmonary ventilation
57
how is O2 delivered to the muscle?
blood flow and O2 content
58
how is O2 extracted from the blood?
delivery and Po2 gradient between blood/cell/mitochondria
59
how do blood gases change during exercise?
* High exercise levels – arterial PaO2 declines slightly * As O2 consumption rises, PaO2 in the mixed venous blood also declines * Partial pressure of CO2 rises * Arteriovenous difference in O2 content rises * Increase in gradient drives O2 diffusion into cells
60
why is there reduced affinity of Hb for O2 during exercise?
* Increased CO2 * Increase H+ * Increase in temperature
61
what effect does reduced affinity of Hb for O2 have on O2 delivery to tissues?
increases O2 delivery to the tissues
62
define excess post-exercise oxygen comsumption
measurable increase in the rate of oxygen intake/uptake following strenuous activity
63
how does the body build up an oxygen deficit?
* O2 consumption doesn’t rise immediately – rises over several mins until it matches the needs of the exercising muscles * As work continues, O2 uptake remains at a level that’s appopriate for exercise levels
64
why is EPOC needed?
eliminates O2 debt
65
what is made during the initial phase of O2 decline?
ATP and creatine phosphate are resynthesised via oxidative pathways • Excess lactate is resynthesised into glucose and glycogen
66
what causes changes to HR and contraction force occur after autonomic factors?
* Changes bc of signals from central command of the brain * Central command acts to regulate baroreceptor reflex sensitivity * CC also gets feedback from increased activity in afferent nerves from exercising limbs * Metaboreceptors respond to changes in metabolite concentrations (mainly pH + K+)
67
what mechanisms activate respiratory muscles?
neural mechanisms
68
what part of the brain causes an increase n ventilation?
initiation of motor activity from premotor area of the cerebral cortex chemoreceptors also contribute
69
what is the major driver for ventilation?
CO2
70
what effect does a denervated carotid body have on patients?
they have slower ventilatory responses
71
what effect do elevated potassium concentrations have on the body during exercise?
thought to provide an extra stimulus to peripheral chemoreceptors.

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